Version July 2025
Elevated intraocular pressure: Ophthalmic:
Solution: Instill 1 to 2 drops into affected eye(s) twice daily.
Suspension (Betoptic S): Instill 1 drop into affected eye(s) twice daily.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling.
There are no dosage adjustments provided in the manufacturer's labeling.
Refer to adult dosing.
(For additional information see "Betaxolol (ophthalmic): Pediatric drug information")
Elevated intraocular pressure: Infants, Children, and Adolescents: Ophthalmic suspension (Betoptic S): Instill 1 drop into affected eye(s) twice daily
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Infants, Children, and Adolescents: There are no dosage adjustments provided in manufacturer's labeling (has not been studied).
Infants, Children, and Adolescents: There are no dosage adjustments provided in manufacturer's labeling (has not been studied).
The following adverse drug reactions are derived from product labeling unless otherwise specified.
Frequency not defined:
Cardiovascular: Altered blood pressure
Ophthalmic: Eye discomfort (transient)
Postmarketing:
Cardiovascular: Bradycardia, heart block, heart failure
Dermatologic: Alopecia, toxic epidermal necrolysis, urticaria
Gastrointestinal: Dysgeusia, glossitis
Nervous system: Altered sense of smell, depression, dizziness, exacerbation of myasthenia gravis, headache, insomnia, lethargy, vertigo
Ophthalmic: Blurred vision, crusting of eyelash, decreased visual acuity, dry eye syndrome, eye discharge, eye pain, eye pruritus, eye redness, foreign body sensation of eye, lacrimation, ophthalmic inflammation, photophobia, superficial punctate keratitis
Respiratory: Respiratory distress (including asthma, bronchospasm, dyspnea, respiratory failure, thickening of bronchial secretions)
Hypersensitivity to betaxolol or any component of the formulation; sinus bradycardia; atrioventricular block greater than first-degree; cardiogenic shock; uncompensated cardiac failure.
Canadian labeling: Additional contraindications (not in US labeling): Reactive airway disease including bronchial asthma or a history of bronchial asthma; severe chronic obstructive pulmonary disease (COPD); sick sinus syndrome sino-atrial block
Concerns related to adverse events:
• Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.
Disease-related concerns:
• Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; if used at all, should be used cautiously with close monitoring; asthma exacerbation and pulmonary distress has been reported during betaxolol use.
• Cardiovascular insufficiency: Use with caution in patients with cardiovascular insufficiency; if signs of decreased cerebral blood flow occur, consider alternative therapy.
• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms.
• Heart failure: Use with caution in patients with compensated heart failure (HF) and monitor for a worsening of the condition. Discontinue at the first signs of cardiac failure. In a scientific statement from the American Heart Association, betaxolol has been determined to be an agent that may exacerbate underlying myocardial dysfunction (magnitude: major) (AHA [Page 2016]).
• Myasthenia gravis: Use with caution in patients with myasthenia gravis; may worsen disease.
• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If thyrotoxicosis is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm.
• Vascular insufficiency: Use with caution in patients with vascular insufficiency due to potential effects on blood pressure and pulse; if signs/symptoms of reduced cerebral blood flow or Raynaud phenomenon (RP) develop during therapy, consider alternative therapy.
Special populations:
• Contact lens wearers: Ophthalmic solution/suspension contains benzalkonium chloride which may be absorbed by contact lenses; remove contact lens prior to administration and wait 15 minutes before reinserting.
Dosage form specific issues:
• Ophthalmic: Inadvertent contamination of multiple-dose ophthalmic solutions has caused bacterial keratitis. Should not be used alone in angle-closure glaucoma (has no effect on pupillary constriction). Choroidal detachment has been reported with aqueous suppressant therapy after filtration procedures.
Other warnings/precautions:
• Absorption: Systemic absorption of betaxolol and adverse effects may occur with ophthalmic use, including severe respiratory and cardiac reactions.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution, Ophthalmic:
Generic: 0.5% (5 mL, 10 mL, 15 mL)
Suspension, Ophthalmic:
Betoptic-S: 0.25% (10 mL [DSC], 15 mL [DSC])
Betoptic-S: 0.25% (10 mL, 15 mL) [contains benzalkonium chloride, edetate (edta) disodium]
May be product dependent
Solution (Betaxolol HCl Ophthalmic)
0.5% (per mL): $12.33
Suspension (Betoptic-S Ophthalmic)
0.25% (per mL): $48.68
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Suspension, Ophthalmic:
Betoptic-S: 0.25% (5 mL, 10 mL) [contains benzalkonium chloride, edetate (edta) disodium]
Ophthalmic: Shake suspension well before using. Tilt head back and instill in eye. Keep eye open and do not blink for 30 seconds. Apply gentle pressure to lacrimal sac for 1 minute. Wipe away excess from skin. Do not touch applicator to eye and do not contaminate tip of applicator. Administer other ophthalmic agents at least 10 minutes prior to instilling betaxolol products.
Ophthalmic: Administer other topically applied ophthalmic medications at least 10 minutes before Betoptic S; wash hands before use; shake well before administration; do not allow the dispenser tip to touch the eye. Apply gentle pressure to lacrimal sac during and immediately following instillation (1 minute) or instruct patient to gently close eyelid after administration to decrease systemic absorption of ophthalmic drops (Ref). Some solutions contain benzalkonium chloride; wait at least 15 minutes after instilling solution before inserting soft contact lenses.
Elevated intraocular pressure: Treatment of elevated intraocular pressure in patients with chronic open-angle glaucoma or ocular hypertension.
Betoptic S may be confused with Betagan, Timoptic
Substrate of CYP1A2 (Minor), CYP2D6 (Minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential;
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Acetylcholinesterase Inhibitors: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Alpha2-Agonists: Beta-Blockers may increase rebound hypertensive effects of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Alpha2-Agonists may increase AV-blocking effects of Beta-Blockers. Sinus node dysfunction may also be enhanced. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Risk D: Consider Therapy Modification
Amiodarone: May increase bradycardic effects of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase serum concentration of Beta-Blockers. Risk C: Monitor
Antidiabetic Agents: Beta-Blockers (Beta1 Selective) may increase adverse/toxic effects of Antidiabetic Agents. Specifically, beta-blockers may mask the hypoglycemic symptoms of antidiabetic agents. Risk C: Monitor
Antipsychotic Agents (Phenothiazines): May increase hypotensive effects of Beta-Blockers. Beta-Blockers may decrease metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease metabolism of Beta-Blockers. Risk C: Monitor
Beta2-Agonists: Beta-Blockers (Beta1 Selective) may decrease bronchodilatory effects of Beta2-Agonists. Of particular concern with nonselective beta-blockers or higher doses of the beta1 selective beta-blockers. Risk C: Monitor
Bradycardia-Causing Agents: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Cafedrine: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Cafedrine. Risk C: Monitor
Cannabis: Beta-Blockers may increase adverse/toxic effects of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor
Ceritinib: Bradycardia-Causing Agents may increase bradycardic effects of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider Therapy Modification
Cholinergic Agonists: Beta-Blockers may increase adverse/toxic effects of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Risk C: Monitor
Dipyridamole: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Disopyramide: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may increase negative inotropic effects of Disopyramide. Risk C: Monitor
DOBUTamine: Beta-Blockers may decrease therapeutic effects of DOBUTamine. Risk C: Monitor
Dronedarone: May increase bradycardic effects of Beta-Blockers. Dronedarone may increase serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Increase monitoring for clinical response and adverse effects. Risk D: Consider Therapy Modification
EPHEDrine (Systemic): Beta-Blockers may decrease therapeutic effects of EPHEDrine (Systemic). Risk C: Monitor
EPINEPHrine (Nasal): Beta-Blockers (Beta1 Selective) may decrease therapeutic effects of EPINEPHrine (Nasal). Risk C: Monitor
EPINEPHrine (Oral Inhalation): Beta-Blockers (Beta1 Selective) may decrease therapeutic effects of EPINEPHrine (Oral Inhalation). Risk C: Monitor
EPINEPHrine (Systemic): Beta-Blockers (Beta1 Selective) may decrease therapeutic effects of EPINEPHrine (Systemic). Risk C: Monitor
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may increase vasoconstricting effects of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor
Etilefrine: Beta-Blockers may decrease therapeutic effects of Etilefrine. Etilefrine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Etofylline: Beta-Blockers may decrease therapeutic effects of Etofylline. Risk X: Avoid
Etrasimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Fexinidazole: Bradycardia-Causing Agents may increase arrhythmogenic effects of Fexinidazole. Risk X: Avoid
Fingolimod: Bradycardia-Causing Agents may increase bradycardic effects of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider Therapy Modification
Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may increase adverse/toxic effects of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider Therapy Modification
Isoproterenol: Beta-Blockers may decrease therapeutic effects of Isoproterenol. Risk C: Monitor
Ivabradine: Bradycardia-Causing Agents may increase bradycardic effects of Ivabradine. Risk C: Monitor
Lacosamide: Bradycardia-Causing Agents may increase AV-blocking effects of Lacosamide. Risk C: Monitor
Landiolol: Bradycardia-Causing Agents may increase bradycardic effects of Landiolol. Risk X: Avoid
Mavacamten: Beta-Blockers may increase adverse/toxic effects of Mavacamten. Specifically, negative inotropic effects may be increased. Risk C: Monitor
Methacholine: Beta-Blockers may increase adverse/toxic effects of Methacholine. Risk C: Monitor
Midodrine: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Mivacurium: Beta-Blockers may increase therapeutic effects of Mivacurium. Risk C: Monitor
NIFEdipine (Topical): May increase adverse/toxic effects of Beta-Blockers. Risk C: Monitor
NIFEdipine: May increase hypotensive effects of Beta-Blockers. NIFEdipine may increase negative inotropic effects of Beta-Blockers. Risk C: Monitor
Nitrendipine: May increase therapeutic effects of Beta-Blockers. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents (Topical): May decrease therapeutic effects of Beta-Blockers. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents: May decrease antihypertensive effects of Beta-Blockers. Risk C: Monitor
Opipramol: Beta-Blockers may increase serum concentration of Opipramol. Opipramol may increase serum concentration of Beta-Blockers. Risk C: Monitor
Ozanimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Ponesimod: Bradycardia-Causing Agents may increase bradycardic effects of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider Therapy Modification
Reserpine: May increase hypotensive effects of Beta-Blockers. Reserpine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Rivastigmine: May increase bradycardic effects of Beta-Blockers. Risk X: Avoid
Siponimod: Bradycardia-Causing Agents may increase bradycardic effects of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider Therapy Modification
Succinylcholine: Beta-Blockers may increase neuromuscular-blocking effects of Succinylcholine. Risk C: Monitor
Tasimelteon: Beta-Blockers may decrease therapeutic effects of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider Therapy Modification
Theodrenaline: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Theodrenaline. Risk C: Monitor
Theophylline Derivatives: Beta-Blockers (Beta1 Selective) may decrease bronchodilatory effects of Theophylline Derivatives. Risk C: Monitor
White Birch Allergen Extract: Beta-Blockers may increase adverse/toxic effects of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid
When administered orally, betaxolol crosses the placenta and can be detected in the amniotic fluid and umbilical cord blood (Morselli 1990).
The amount of betaxolol available systemically following topical application of the ophthalmic drops is significantly less in comparison to oral doses (Vainio-Jylhä 2001). However, the same adverse effects observed with systemic administration may occur. If ophthalmic agents are needed during pregnancy, the minimum effective dose should be used in combination with punctal occlusion to decrease potential exposure to the fetus (Johnson 2001; Salim 2014; Samples 1988).
It is not known if betaxolol is present in breast milk following ophthalmic administration.
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother. The minimum effective dose should be used in combination with punctual occlusion to decrease potential exposure to the breastfeeding infant (Johnson 2001; Salim 2014; Samples 1988).
Intraocular pressure
Competitively blocks beta1-receptors, with little or no effect on beta2-receptors; with ophthalmic use, reduces intraocular pressure by reducing the production of aqueous humor
Onset of action: Within 30 minutes
Peak effect: Intraocular pressure reduction: ~2 hours
Duration: ≥12 hours
Absorption: Rapidly absorbed into the systemic circulation (concentrations ~1/10 to 1/20 of oral dosing) (Vainio-Jylhä, 2001)
Excretion: Urine (>80%, as unchanged drug [15%] and inactive metabolites)
